Promotion of cell proliferation by the proto-oncogene DEK enhances oral squamous cell carcinogenesis through field cancerization

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11289
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Gifu University
• Principal Investigator: TOMITA HIROYUKI 岐阜大学, 大学院医学系研究科, 准教授 (50509510)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 口腔癌 / DEK / 扁平上皮癌

Outline of Final Research Achievements

Oral squamous cell carcinoma (OSCC) develops through a multistep carcinogenic process involving field cancerization. DEK overexpression is associated with malignancies; however, the functional roles of DEK overexpression are unclear. We demonstrated that DEK-expressing cells were significantly increased in human dysplasia/carcinoma in situ and OSCC. Furthermore, we generated ubiquitous and squamous cell-specific doxycycline (DOX)-inducible Dek mice (iDek and iDek-e mice respectively). Both DOX+ iDek and iDek-e mice did not show differences in the oral mucosa compared with DOX- mice. In the environment exposed to carcinogen, DOX-treated (DOX+) iDek mice showed field cancerization and OSCC development. Microarray analysis revealed that DEK overexpression was mediated by the upregulation of DNA replication- and cell cycle-related genes, particularly those related to the G1 /S transition. T

Free Research Field

腫瘍病理